Inflammation-set to fire; Latin: inflammare

Acute inflammation is a short-term response that usually results in healing:

leukocytes infiltrate the damaged region, removing the stimulus and
repairing the tissue.
Chronic inflammation, by contrast, is a prolonged, dysregulated and
maladaptive response that involves active inflammation, tissue destruction
and attempts at tissue repair. Such persistent inflammation is associated with
many chronic human conditions and diseases, including allergy,
atherosclerosis, cancer, arthritis and autoimmune diseases.

Bodys Immediate and Normal and Necessary and Non-specific (irrespective of

cause of injury) response to any tissue injury
Definition:
Complex response of vascularised tissues? (avascular tissues? Cornea?) to tissue
injury or infection, which brings cells and molecules of host defence from circulation
to sites of need, to restore the tissue to its pre-injury state and/or eliminate the
offending agents
It consists of a dynamic complex of histologically apparent cytologic changes,
cellular infiltration and mediator release in the affected blood vessels and adjacent
tissues
It is actually a physiological protective response, but can be pathological also, as
in chronic inflammation or SIRS or autoimmune diseases like rheumatoid arthritis,
when it is inappropriately triggered or poorly controlled
Local inflammatory response -> inflammatory mediators -> too much -> systemic
effects can occur
Cardinal features of inflammation:
1.
2.
3.
4.
5.

Rise in temperature (Callor)

Pain (Dollor)
Redness (Rubor)
Swelling (Tumor/Edema)
Loss of function (Functio laesa)

Regardless of mechanism of injury, same physiological cause, same response

Inflammation of a tissue/organ -itis; often infections are accompanied by
inflammation
Purpose:

To get rid of initial cause of inflammation (like microbes or foreign particles)

To get rid of the consequences of injury (like damaged tissue debris)
To initiate the process of repair/wound healing
Enables the bodys defensive and regenerative resources to be channelled
into tissues which have suffered damage or are contaminated, so as to limit

the damaging effect of the contaminant and eliminate both the contaminant
as well as the injured tissue debris and promote healing process.
If inflammation didnt happen: any natural/acquired medical conditions? Steroid
therapy?

Infections could not be restrained

Wound healing would not take place; injured tissue remain as suppurative
sores

Causes:

Infection (direct effect of endotoxins from microbes or secondary to activation

of immune system)
Immunological (Autoimmune disease - rheumatoid arthritis, type1 DM/Allergy
bronchial asthma)
Tissue Necrosis as a result of :
o Physical injury - Trauma (cut, crushed, bruising, friction, pressure),
Thermal causes (too hot/too cold), Radiation (delayed inflammatory
response-sunburn?)
o Chemical agents (acid/alkali e.g. GERD, peritonitis, pancreatitis, alcoholic
gastritis)
o Ischemia /Hypoxia

Inflammatory process: Acute inflammation

Rapid in onset and short term response

Results in repair/wound healing
Mediated by a Local release of chemical inflammatory mediators
When first insulted, a very transient vasoconstriction? followed by pronounced
vasodilatation occurs - vascular response
This is followed by the migration of neutrophils and monocytes, from the blood
vessels into the injured tissue - cellular response

Vascular response-results of vasodilatation

Permeability (more exudation of plasma): In vasodilatation, the cells dont grow
big/stretch, the intercellular spaces and gaps just get bigger
1. More nutrients (glucose-energy, vitc-collagen, amino acids-cellular proteins, fatty
acids-cell membranes etc..)-> needed for the anabolic healing process;
2. Dilution effect on the bacterial toxins
3. Fibrinogen move out, form insoluble fibrin in the tissue and compartmentalize it,
separating the area from the rest of the body
4. Inflammatory mediators increase the sensitivity of the nociceptors in the tissue
-> hyperalgesia
Hyperemia (more blood flow):

1. Provides more oxygenation -> meeting the demand from anabolic processes
required -> for repair/ new cells
2. Increased flow of blood especially diverted from the core flow -> increased
temperature
*Clinics: Is this wound getting good oxygenation/ perfusion? Its needed for proper
fast healing! Bacterial endotoxins and substances prevent wound healing, it can be
present for years as chronic inflammation, but wont heal-antibiotics and cleaning
must!
Cellular response
Migration of WBCs into the tissue - margination, rolling, squeeze out
Neutrophils and Macrophages eat up the bugs as well as dead cells (ideal niche for
bacterial growth, also, wound healing cant occur over dead cells, need space)
Inflammatory mediators:
Groups of proteins and chemicals that stimulate and choreograph the inflammatory
response
3 types:

Prostaglandin type of mediators

Locally released Vasoactive chemicals
Cytokines

Prostaglandins
Phospholipids (from injured cells) -(tissue Phospholipase A)-> Arachidonic acid
(tissue COX)-> PGAs
*Clinically: Steroids like prednisolone inhibit Phospholipase A, have potent antiinflammatory effects; NSAIDs like ibuprofen, aspirin, diclofenac inhibit COX have
similar anti-inflammatory effects
Vasoactive chemicals
Plasma-derived, Platelet-derived, Endothelium-derived, Complement system, Mast
cell-derived (histamine)
Cytokines
Cytokines mediating inflammation are mainly produced by macrophages and
lymphocytes like TNF
If a large area of tissue is inflamed, then an overall systemic effect takes place
called systemic inflammatory response syndrome (SIRS) /acute phase response
Systemic effects:
Criteria for SIRS/APR

Fever/pyrexia >38 (immune system works most efficiently at pyrexia

temperatures)
Tachycardia >90
Tachypnoea >20(increased oxygen requirement to meet the increased
metabolic rate in pyrexia)
Leukocytosis

SIRS resulting from infective causes called SEPSIS

(2 additional criteria for sepsis: Altered mental state + Hyperglycemia)

Cytokines cause muscle cell protein catabolism to release amino acids to

build up immunoglobulins and repair damaged tissue (aching muscles)
Cytokines act on the appetite centre (anorexia)
Cytokines act on the CNS (lethargy)

Causes of SIRS:

Ischemic causes
Reperfusion causes
Trauma, burns
Chemical injury
Infection Sepsis -> severe sepsis (+organ failure) -> septic shock
(+hypotension, hypoperfusion)

Inflammation of -itis:
Rhinitis
Bronchitis

Arthritis
(joints)

Encephalitis

Meningitis
Poliomyelitis
Pneumonitis
Endocarditis
(nerves)
(alveoli)
Myocarditis
Cellulitis
Osteomyeliti
Gingivitis
s (medullary Conjunctiviti
cavity)
s
Glossitis
Tendonitis

Dermatitis

Tonsilitis

Laryngitis

Cholecystitis Prostatitis

Esophagitis

Peritonitis

Gastritis

Labyrinthitis

Gastroenteri Otitis
tis
Salpingitis
Appendicitis
Vulvitis
Colitis
Balanitis
Pancreatitis

Pyelonephrit
is
Urethritis
Cystitis
(urinary
bladder)
Vasculitis

Outcomes of inflammation:

Resolution
Scaring (severe massive inflammation)
Abscess formation with pus (Chronic inflammation)

Some terms:

Suppurative pus producing

Purulent pus filled
Empyema pus filled cavity